Also not a doctor, but my dad has lung cancer (never smoked, just a "surprise, stage 4 lung cancer").

Specifically, he has the ALK mutation. This occurs in 3-5% of non small cell lung cancers.

He's on an inhibitor drug (a successor to Crizotinib) for this specific mutation. These drugs turned a ~6 month prognosis into a 5 year prognosis. But this set of drugs only works on this specific mutation. The cancer eventually mutates around the drug.

State of the art cancer drugs are really amazing, but they're still so far away from a cure.

Perhaps this is how we'll eventually manage cancer. By frequent testing and moving from drug to drug as cancer sheds one mutation and adapts other one, turning cancer into manageable state.

Yep, I think manage is the right way to put it.

Fundamentally, viewing cancer as whole bunch of different adaptive adversaries as opposed to a single disease is probably correct. Under that view, consider 'cancer' as the mathematical outcome of the genes in the cells in your body attempting to revert to their fundamentally selfish nature and greedily replicate as much as possible. Every gene in your genome got there because its ancestor genes managed to replicate (though perhaps with a mutation or 2 along the way).

So perhaps it's helpful to think of the organism as a giant prison of small bits of self replicating code (genes). Several checks are in place to ensure that no bit of code replicates beyond sane bounds. However every once in a while a guard get's knocked out or cellblock door switch is left unattended, or a prisoner disguises itself, or groups up with another to overpower or sidestep an existing control mechanism. And then it's off to the races. Higher levels of control can attempt to rectify the situation, but they can fail as well. Given that your body has 100 trillion cells, and about 20 thousand genes. You are talking about a 2 quintillion protein synthesizing programs executing, all of them are there for one reason, they had ancestors that were able to reproduce themselves. They don't have any notion of a greater good, or a serving their purpose or any of that. They can't be reasoned with, they are an adaptive chemical reaction, that either doesn't replicate, or does (and perhaps so much so that it takes down the whole system).

So a lot of cancer treatment are going to revolve around, at our level of technology:

- the ability to target specific classes of cells with certain noisy markers, which may or may not be reachable and with a lot of collateral damage and which contain the errant genes and killing them. (e.g. clusters of cells showing up as a visible tumor in an x-ray, cells having certain chemical signatures)

- the ability to deprive (all or better yet classes of) cells of what they need to replicate to slow them down and potentially eventually have them die off taking the cancerous genes with them.

- the ability to shore-up or reactivate compromised internal defenses.

As well as prevention methods such as:

- avoiding weakening systems that protect against replication (e.g. )

- avoiding encouraging massive amounts of mutation (e.g. repetitive inflammation or free radicals or radiation exposure like UV rays or cesium-137 )

...etc

Are any one of these things going to cure cancer? No, they aren't anymore than telling C programmer to use strncpy instead of strcpy is going to stop all buffer overflow attacks, which in turn prevents remote code execution, which in turn prevents botnets. Or marking all attachments to emails as un-executable is going to stop all computer viruses.

But every bit helps, and saves countless lives, gradually this wack-a-mole approach has shown results.

In the future, perhaps it'll be possible to solve cancer by scanning every cell in the body and selectively eliminating cells that fail some basic sanity checks. We aren't at that point yet, but if we were we would have a pretty effective cancer treatment. It would be adding another (very effective) layer on top of all the other systems walking the day to day beat and slowing stuff down. I'd hesitate to call it a cure though, because if it was halted it would just be a matter of time until one of the selfish genes blindly do their replication thing a little to well for everyone's good.

I'm probably not more knowledgeable, but from my understanding, most (all?) cancers are related in that they start as a single mutated cell which replicates in an aggressive way which leads to problems / death.

Since it's a mutated cell, I can imagine extracting DNA from the cancerous area, and doing a diff against your "normal" DNA from elsewhere in your body. This would enable you to identify the difference / unique signature of the cancerous cells, kind of how a software antivirus looks for binary patterns in things that it scans. A mechanism like CRISPR could then be used to effectively target all instances of the mutated DNA / cells in your body, effectively wiping it out.

I suspect this is ridiculously hand-wavy and oversimplified, but something like this might just be viable in our lifetimes.

Parts of this are already possible.

A challenge, though, is that cancer cells tend to have wildly unstable genomes.

Further reading - with good summaries of current thinking: - https://en.wikipedia.org/wiki/Hallmarks_of_cancer - https://en.wikipedia.org/wiki/Two-hit_hypothesis

I think a very interesting research area is to find the core (original, required) mutations involved in a cancer (the current understanding is that normally multiple mutations are required, occurring in a particular progression).

I thought that there's constantly countless cells in your body with genetic mutations. Most just have benign effects.

I'd better research this a bit more.

Interesting keyword to research: "p53".

Example (very readable): https://www.amazon.co.uk/dp/B00NB14L6Y

> If a cell makes a mistake in copying its DNA during the process of division, p53 stops it in its tracks, summoning a repair team before allowing the cell to carry on dividing. If the mistake is irreparable and the rogue cell threatens to grow out of control, p53 commands the cell to commit suicide. Cancer cannot develop unless p53 itself is damaged or prevented from functioning normally.

Thank you! That's something I wouldn't have discovered so easily and makes my learning about it much easier.

The current hypothesis is that it is similar to bacterial antibiotic escape. Effectively the cells are growing rapidly and acquire mutations. This is why you want to treat with combination chemotherapy. However, there are some big issues. First, we only test drugs in isolation and then sometimes they will try two together after a long long time. This is how leukemia achieved high remission rates back back in the wild wild west days. Today there is a focus on targeted chemotherapies and then of course the holy grail of immunotherapy. I hope we figure out how to program the immune system to great effect. That and viral targeting therapies that use crisper. But these are early days and progress cannot come fast enough.

Basically this. Even though there isn't one particular cure all solution, there are many more treatments available which are more effective than in the past.

The article discussed finding targets expressed by different cancers.

The main problem is that a cancer can be quite heterogeneous. You really need multiple ways of killing a given cancer to be certain all is gone.